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AI-Powered Test Automation: Embracing the Future of Software Testing – TechDecisions

Last year, the global pandemic caused a major shift in how businesses operate, introducing new challenges of remote work and accelerated digital transformation at an unprecedented pace.

Organizations are now in a race against time to build high-quality software to propel their digital transformation initiatives forward. However, ensuring optimal software quality in a fast-paced, hyper-connected and complex world is not an easy task.

While traditional test automation has enabled test teams with a smarter and quicker means for delivering high software quality, AI-powered tools can drive its capabilities to the next level.

Traditional test automation delivers tools to control test execution and compare test results against expected outcomes.

While such tools can test and deliver results automatically, they still need human supervision. Without human supervision, traditional test automation tools cant identify which tests to run, so they end up running every test or a predetermined set of tests.

When powered by AI, a test automation tool can review the current test status, recent code changes, code coverage and other associated metrics to intelligently decide which tests to run and then trigger them automatically.

Read: How Intelligent Automation is Changing Global Business

AI enables test automation to move beyond its scope of simple rule-based automation. It utilizes AI algorithms to efficiently train systems using large data sets.

Through the application of reasoning, problem-solving and machine learning, an AI-powered test automation tool can mimic human behavior and reduce the direct involvement of software testers in mundane tasks.

AI is changing software testing in many ways. It is removing many limitations in traditional test automation and delivering more value to testers and developers alike.

It enables organizations to test faster and better while reducing costs and human dependencies. AI has imparted an incredible positive impact on most software testing use cases, including:

Unit TestingTesters can use RPA tools (an application of AI) to reduce flaky test cases while conducting unit testing. Such tools can also help with the maintenance of unit test scripts.API TestingAI-powered test automation tools can convert manual UI tests into automated API tests. This lowers the requirement of specialized testing skills for the process and enables organizations to build a more sustainable API testing strategy.

Read: You Need Predictive Analytics for Your Software Testing: Heres Why

UI TestingEnsures more accuracy in comparison to manual testing. It is hard to manually detect parameters such as GUI size difference and a combination of colors, which can be easily identified with AI.

Regression TestingEnables test teams to run the entire test suite in a timely manner on every change, however minor it may be. AI can prioritize and re-target regression tests to test high-risk areas with short run-times. Image-Based TestingVisual validations involved in image-based testing can be simplified with the ML capability of AI. Automated visual validation tools make image-based testing a breeze.

Like any new technology, there is a lot of hype around AI-powered software testing. The utilization of AI in various testing scenarios is delivering significant improvements and making intelligent test automation a reality. AI-powered test automation is helping organizations reimagine software testing and delivering real business benefits. Some of its key benefits for organizations include:

1. Auto-Generation of Test Scripts

AI-powered test automation helps teams with the auto-generation of test codes that perform all the required functions, such as click buttons, form fills, app logins and more.

There will be complex test cases for which AI-powered test automation tools cant generate code, but it can auto-generate more than 80% of the required code reliably, enhancing the productivity of testing teams significantly.

Furthermore, AI also helps with auto-maintenance to ensure continuous quality while reducing the burden on human testers.

2. Optimization of Testing Process

AI is the force behind the product recommendations on Amazon or the shows Netflix suggests. An AI-enabled recommendation engine allows marketers to provide relevant product recommendations to customers in real-time.

The same approach can be applied to simplify software testing. AI can suggest tests with the maximum probability of finding bugs, based on the risk information, removing the guesswork from testing and empowering teams to home in on the actual risk areas.

3. Measurement of Release Impact

AI-powered test automation tools can predict how an upcoming software release will impact end-users.By leveraging neural networks and analyzing test history and data from current test runs, the tool can predict whether customer satisfaction will move up or down. Equipped with such information, organizations can adjust likewise and ensure that their customers remain satisfied with the user experience.

4. Delivers a Competitive Edge

AI-powered test automation tools help organizations gain a competitive edge. Various AI capabilities such as ML and neural networks can be used to understand how various technical factors are impacting the user experience and business outcomes.

For example, AI can detect whether a new implementation is negatively impacting the load times and could lower conversion rates upon release.

By delivering predictions on how releases will affect the business, AI-powered tools empower organizations to make course corrections to have a positive impact.

5. Enables Productivity and Cost Gains

A recent study discovered that testers spend 17% of their time dealing with false positives and another 14% on additional test maintenance tasks. An AI-powered tool with its auto-generation and auto-maintenance capabilities can help test teams save valuable time and effort and put it toward tackling complex requirements.

It can also help organizations optimize testing costs by reducing human dependence on mundane testing tasks.

Its quite clear that AI-powered test automation is not a passing fad. Such tools are enabling organizations to understand and adapt better to ever-changing customer expectations. Rather than taking a wait-and-watch approach, its time to embrace the innovation that AI has unleashed in test automation.

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AI-Powered Test Automation: Embracing the Future of Software Testing - TechDecisions

Optic nerve firing may spark growth of vision-threatening childhood tumor – National Institutes of Health

News Release

Tuesday, June 1, 2021

NIH-funded pre-clinical study supports key role of neural activity in brain cancers.

In a study of mice, researchers showed how the act of seeing light may trigger the formation of vision-harming tumors in young children who are born with neurofibromatosis type 1 (NF1) cancer predisposition syndrome. The research team, funded by the National Institutes of Health, focused on tumors that grow within the optic nerve, which relays visual signals from the eyes to brain. They discovered that the neural activity which underlies these signals can both ignite and feed the tumors. Tumor growth was prevented or slowed by raising young mice in the dark or treating them with an experimental cancer drug during a critical period of cancer development.

Brain cancers recruit the resources they need from the environment they are in, said Michelle Monje, M.D., Ph.D., associate professor of neurology at Stanford University, Palo Alto, California, and co-senior author of the study published in Nature. To fight brain cancers, you have to know your enemies. We hope that understanding how brain tumors weaponize neural activity will ultimately help us save lives and reduce suffering for many patients and their loved ones.

The study was a joint project between Dr. Monjes team and scientists in the laboratory of David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor and the director of the Neurofibromatosis Center at the Washington University School of Medicine in St. Louis.

In 2015, Dr. Monjes team showed for the first time that stimulation of neural activity in mice can speed the growth of existing malignant brain tumors and that this enhancement may be controlled by the secretion of a protein called neuroligin-3. In this new study, the researchers hoped to test out these ideas during earlier stages of tumor development.

Over the years, cancer researchers have become more and more focused on the role of the tumor microenvironment in cancer development and growth. Until recently, neuronal activity has not been considered, as most studies have focused on immune and vascular cell interactions, said Jane Fountain, Ph.D., program director at the NIHs National Institute of Neurological Disorders and Stroke (NINDS), which partially funded the study. This study is one of the first to show a definitive role for neurons in influencing tumor initiation. Its both scary and exciting to see that controlling neuronal activity can have such a profound influence on tumor growth.

Specifically, the researchers chose to study optic nerve gliomas in mice. Gliomas are formed from newborn cells that usually become a type of brain cell called glia. The tumors examined in this study are reminiscent of those found in about 15-20% of children who are born with a genetic mutation that causes NF1. About half of these children develop vision problems.

Dr. Gutmann helped discover the disease-causing mutation linked to NF1 and its encoded protein, neurofibromin, while working in a lab at the University of Michigan, Ann Arbor, which was then led by the current NIH director, Francis S. Collins, M.D., Ph.D. Since then, the Gutman teams pioneering work on NF1, and particularly NF1-brain tumors, has greatly shaped the medical research communitys understanding of low-grade glioma formation and progression.

Based on multiple lines of converging evidence, we knew that these optic nerve gliomas arose from neural precursor cells. However, the tumor cells required help from surrounding non-cancerous cells in the optic nerve to form gliomas, said Dr. Gutmann, who was also a senior author of this study. While we had previously shown that immune cells, like T-cells and microglia, provide growth factors essential for tumor growth, the big question was: What role did neurons and neural activity play in optic glioma initiation and progression?

To address this, the researchers performed experiments on mice engineered by the Gutmann laboratory to generate tumors that genetically resembled human NF1-associated optic gliomas. Typically, optic nerve gliomas appear in these mice between six to sixteen weeks of age.

Initial experiments suggested that optic nerve activity drives the formation of the tumors. Artificially stimulating neural activity during the critical ages of tumor development enhanced cancer cell growth, resulting in bigger optic nerve tumors. In contrast, raising the mice in the dark during that same time completely prevented new tumors from forming.

Interestingly, the exact timing of the dark period also appeared to be important. For instance, two out of nine mice developed tumors when they were raised in the dark beginning at twelve weeks of age.

These results suggest there is a temporal window during childhood development when genetic susceptibility and visual system activity critically intersect. If a susceptible neural precursor cell receives the key signals at a vulnerable time, then it will become cancerous. Otherwise no tumors form, said Yuan Pan, Ph.D., a post-doctoral fellow at Stanford and the lead author. We needed to understand how this happens at a molecular level.

Further experiments supported the idea that neuroligin-3 may be a key player in this process. For instance, the scientists found high levels of neuroligin-3 gene activity in both mouse and human gliomas. Conversely, silencing the neuroligin-3 gene prevented tumors from developing in the neurofibromatosis mice.

Traditionally, neuroligin-3 proteins are thought to act like tie rods that physically brace neurons together at communication points called synapses. In this study, the researchers found that the protein may work differently. The optic nerves of neurofibromatosis mice raised under normal light conditions had higher levels of a short, free-floating version of neuroligin-3 than the nerves of mice raised in the dark.

Previously our lab showed that neural activity causes shedding of neuroligin-3 and that this shedding hastens malignant brain tumor growth. Here our results suggest that neuroligin-3 shedding is the link between neural activity and optic nerve glioma formation. Visual activity causes shedding and shedding, in turn, transforms susceptible cells into gliomas, said Dr. Monje.

Finally, the researchers showed that an experimental drug may be effective at combating gliomas. The drug is designed to block the activity of ADAM10, a protein that is important for neuroligin-3 shedding. Treating the neurofibromatosis mutant mice with the drug during the critical period of six to sixteen weeks after birth prevented the development of tumors. Treatment delayed to twelve weeks did not prevent tumor formation but reduced the growth of the optic gliomas.

These results show that understanding the relationship between neural activity and tumor growth provides promising avenues for novel treatments of NF-1 optic gliomas, said Jill Morris, Ph.D., program director, NINDS.

Dr. Monjes team is currently testing neuroligin-3-targeting drugs and light exposure modifications that may in the future help treat patients with this form of cancer.

This work was supported by grants from the NIH (NS092597, NS111132, NS097211, CA165962, EY026877, EY029137, CA233164); the Department of Defense (W81XWH-15-1-0131, W81XWH-19-1-0260); Brantleys Project supported by Ians Friends Foundation; Gilbert Family Foundation; Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation; Cancer Research UK; Unravel Pediatric Cancer; McKenna Claire Foundation; Kyle OConnell Foundation; Virginia and D. K. Ludwig Fund for Cancer Research; Waxman Family Research Fund; Stanford Maternal and Child Health Research Institute; Stanford Bio-X Institute; Will Irwin Research Fund; Research to Prevent Blindness, Inc.; Schnuck Markets Inc., and Alexs Lemonade Stand Foundation.

This news release describes a basic research finding. Basic research increases our understanding of human behavior and biology, which is foundational to advancing new and better ways to prevent, diagnose, and treat disease. Science is an unpredictable and incremental process each research advance builds on past discoveries, often in unexpected ways. Most clinical advances would not be possible without the knowledge of fundamental basic research. To learn more about basic research at NIH, visit https://www.nih.gov/news-events/basic-research-digital-media-kit.

NINDSis the nations leading funder of research on the brain and nervous system.The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

Pan, Y. et al., NF1 mutation drives neuronal-activity dependent initiation of optic glioma. Nature, May 26, 2021 DOI: 10.1038/s41586-021-03580-6

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Optic nerve firing may spark growth of vision-threatening childhood tumor - National Institutes of Health

40 years of AIDS taught us epidemiologic humility. We need to apply that lesson in fighting Covid-19 – STAT – STAT

Forty years later, I can still recall my visceral reaction to reading an article in the June 5, 1981, issue of Morbidity and Mortality Weekly Report (MMWR), which opened with this sentence: In the period October 1980-May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3 different hospitals in Los Angeles, California.

I was an infectious disease fellow at Harvard Medical School at the time, trying to keep abreast of epidemic trends from the U.S. Centers for Disease Control, which published the weekly bulletin.

One of my first thoughts was that I couldnt believe the MMWR had actually referred to gay men, albeit in the purple prose of the era. It was completely unexpected, since I could not recall the bulletin or the CDC, for that matter ever having discussing sexual and gender minority people before. I was then volunteering once a week at the Fenway Community Health Center which, at the time, was a small neighborhood health clinic not far from Bostons Fenway Park used mostly by gay and bisexual men and transgender women. There, with only limited diagnostics and a fairly rudimentary therapeutic armamentarium, I treated the most challenging presentations of sexually transmitted infections, such as recurrent warts and ulcers.

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When I read the MMWR report, which many herald as the first report of AIDS, I was struck with how the cases described were quite distinctive in that the clinical conditions differed between the men, yet their problems suggested they were severely immunosuppressed without any identifiable cause such as chemotherapy. As a nascent infectious disease specialist, I had a lot of questions, not least of which was how being gay was associated with becoming ill.

The subsequent weeks and months blurred into years of misinformation, false leads, and agonizing deaths. In the earliest days, competing hypotheses for the cause of what was then known as gay-related immune deficiency (GRID) were proposed. The burnout hypothesis suggested that the diversity of illnesses was not due to a single pathogen, but that people who had numerous sexual partners and/or who used many different kinds of drugs were overwhelming their immune systems. Researchers also focused on party drugs such as volatile nitrites (known as poppers), which produced a sense of euphoria and increased sexual pleasure, in an attempt to demonstrate that these drugs were particularly toxic to the immune system.

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As reports emerged of individuals who had never used drugs and/or had few sex partners getting sick because they were sexual partners of individuals who became ill and died, researchers hypothesized that the disease was caused by a transmissible organism. The question then arose as to whether the microbe was a more virulent form of a common existing pathogen, such as ubiquitous herpes simplex, or if AIDS was caused by a new one. The lack of clarity about what was causing AIDS, and the lack of a diagnostic tool that could determine who was sick and who wasnt, fueled hysteria.

In the midst of this uncertainty, the silence of the Reagan administration was palpable, especially when compared to the attention given to the limited number of people who had become sick and died of Legionnaires disease or toxic shock syndrome, two other public epidemics from the 1980s. The implicit message from the administration was that because AIDS seemed to be confined to groups of individuals who didnt matter to society, the less said, the better.

Given what was then known about who was at greatest risk of AIDS and how they might have acquired the infection, people with AIDS also had to contend with high levels of stigma and discrimination. The press routinely referred to AIDS as the 4H disease because it affected Haitians, homosexuals, hemophiliacs, and heroin users.

One of the first patients with AIDS I took care of was a young college student who developed lesions of Kaposi sarcoma that covered his extremities and his face, made his lymph glands swell, and caused fevers, chills, and sweats. As he became sicker and frailer, his parents accompanied him to his medical appointments. His father, a school superintendent, asked perceptive questions about his sons condition. But his son was terrified that any suggestion on my part that he had AIDS would out him to his parents and alienate them from him just when he needed them the most. So I would answer the fathers questions only by saying that his son had a very serious malignancy, and couldnt discuss what was truly going on.

The focus of my research ever since has been HIV and AIDS, primarily how to reduce transmission of the virus. One of the primary lessons Ive learned, however, has little to do with biology: It is how social forces can amplify the transmission of hitherto obscure pathogens. It is clear to me that we will not succeed against SARS-CoV-2 unless we apply the following lessons from the AIDS epidemic:

Science matters. Support for getting people trained to be able to do science matters. Promotion of scientific literacy matters. Science is the creation of new knowledge. There are no such thing as alternative facts. As scientific knowledge expands, so does our understanding of the facts.

Discrimination is toxic. The failure to address the upstream causes of discrimination at the outset of an infectious disease outbreak will make things much worse than they otherwise would be. Homophobia, transphobia, sexism, and racism fueled the HIV epidemic. Racism and economic inequality are fueling the Covid-19 pandemic. The disproportionate impact of Covid-19 infections and health outcomes among people of color in the United States is testament to the urgent need to reduce and eliminate racial and linguistic inequities in scientific research, medical treatment, and disease prevention.

We are all in this together. We live in a global village and share a global gene pool. The HIV epidemic began in Central Africa, and disseminated because of urbanization and increased global mobility. SARS-CoV-2 apparently first appeared in China. But no country owns any virus or other pathogen since the patterns of dissemination of any of these wild organisms depends on human behavior, in addition to intrinsic properties of the pathogen.

AIDS taught us epidemiologic humility: There is only so much we can do. But we can do a lot. Former President George W. Bushs Presidents Emergency Plan for AIDS Relief (PEPFAR) saved millions of lives and is one of the most successful global public health interventions in history. As we scale up to vaccinate increasing numbers of individuals against SARS-CoV-2 in the U.S., Americans must understand that the pandemic is not over here until its over everywhere.

Kenneth H. Mayer is an infectious disease physician, medical research director of Fenway Health, co-director of The Fenway Institute, attending physician in the Division of Infectious Diseases at Beth Israel Deaconess Medical Center, professor of medicine at Harvard Medical School, and professor of global health and population at the Harvard T.C. Chan School of Public Health.

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40 years of AIDS taught us epidemiologic humility. We need to apply that lesson in fighting Covid-19 - STAT - STAT

The Origin of COVID-19 and Preventing the Next Pandemic – War on the Rocks

Did COVID-19 originate with bats or scientists? Most experts continue to contend that the most likely origin of SARS-CoV-2 (the novel coronavirus that causes COVID-19) is a natural zoonotic spillover event between an animal reservoir (most likely bats) and humans. But over the last year of the pandemic, another theory has gained momentum: The SARS-CoV-2 virus may have resulted from an accident in a laboratory in China where scientists were working with closely related viruses. In the wake of the World Health Organization-led mission to Wuhan to examine the origins of the pandemic, proponents of the lab-leak theory have charged the investigative team with conflicts of interest, and suggested that the teams efforts failed to rule out the possibility of a lab release. Some have gone on to claim that scientists have maintained a conspiracy of silence about the possibility of a lab release in order to protect their funding or avoid a backlash from their government.

The desire to identify the origins of the novel coronavirus is perfectly understandable. COVID-19 has killed millions of people and upended everyday life. Theres an intuitive sense that finding out how the pandemic began might help to prevent another one from occurring. The Biden administration is redoubling efforts to determine the origins of COVID-19 after the intelligence community indicated that it had insufficient information to make a determination.

However, while answering the question of where the novel coronavirus came from is important, many of the most important policy decisions the United States needs to make to prevent future pandemics do not depend on viral origins. Very little about pandemic response or preparedness for future pandemics turns on the particulars of how this one started. Laboratory biosafety was already an issue before the pandemic, and the origins of this particular virus dont change the need for reform to prevent these rare but potentially catastrophic events. Regardless of how COVID-19 began, U.S. policy priorities should focus on both identifying and preventing the spread of zoonotic pathogens and bolstering safety and security in high-containment laboratories.

Preparing for the Next Pandemic

Whatever the origins of this pandemic, the United States has its work cut out to prepare for the next one. Lets assume, for the sake of argument, that the lab hypothesis is true. Efforts to prepare for natural spillover events do not then become less important. Since the 1940s, roughly 350 emerging infectious diseases have been identified. Of these, nearly three-quarters have zoonotic origins. Our understanding of how such diseases emerge is incomplete, but we know that there are a number of human behaviors that are likely contributing to this pattern: increasing demand for animal protein, factory farming and other agricultural intensification measures, wildlife trade, urbanization, extraction industries, changes in the food supply chain, and pet ownership, as well as increases in temperature, humidity, and other factors related to global climate change. Zoonotic crossover events are not limited to China, or even to Asia. Emerging infectious diseases have appeared all over the world: Zika in Latin America, Ebola virus disease in sub-Saharan Africa, H1N1 in bird reservoirs as disparate as Vietnam or Mexico; and henipaviruses in Australia. Coronaviruses have reservoirs in China, yes, but also in Africa, the Americas, the Middle East, and Southeast Asia.

If investigators are able to conclusively prove that the COVID-19 pandemic originated in a laboratory conducting research into coronaviruses, humanity will continue to confront the risk that a future spillover will result in another pandemic that is equally or more devastating. Fortunately, there are steps that the scientific community can take to manage this risk, including using predictive surveillance and developing other zoonotic risk-assessment tools. Early detection of such pathogens can help experts to isolate and contain them so that they do not spread widely. We can also promote behavioral change in high-risk populations and fund research into universal vaccines for zoonotic frequent-flyers like coronaviruses.

Lets say the converse is true, however. If evidence is found that satisfies even the most ardent lab-leak proponent that COVID-19 originated in an animal population, does that obviate the need to address laboratory biosafety and biosecurity? Absolutely not. Even as COVID-19 emerged, questions arose about the role of high-containment labs around the world. As the number of these labs increases, the risk of a consequential accident also increases.

Policymakers have debated biological safety in high-containment labs for most of this century. Biosafety, biosecurity, and awareness-raising among life scientists are ongoing topics of discussion at the Biological Weapons Convention. Biosafety is a major focus in the Global Health Security Agenda. The World Health Organization has maintained a guide for the responsible conduct of life sciences research with dual-use potential for more than a decade. In short, biosafety and biosecurity receive significant policymaker attention at the highest levels of international organizations, but that awareness doesnt necessarily translate into national-level action to manage biological risk and ensure protection from accidents. Even the states that have been most vocal in driving discussion of biosafety and biosecurity in international spheres have struggled with their own biorisk management. The United States has had a number of high profile laboratory incidents over the years, involving anthrax, highly pathogenic avian influenza, and smallpox, even as it has continued to develop and expand its high-containment lab capacity already the largest in the world.

Transparency and Biosecurity

Critics might claim that lab releases in the United States can be investigated transparently, while the potential COVID-19 release in China cannot. Indeed, China has put severe restrictions on research into the origins of the virus and prohibited scientists from speaking with journalists. During the World Health Organization-led investigation, members of the team were prevented from accessing patient data and other important research. After Australia pressed for an independent inquiry into the origins of the pandemic, China responded with threats and economic retaliation.

However, opacity surrounding public health is not a problem that is limited to authoritarian societies like China. Globally, biosafety norms are poorly implemented and reviews of biosafety and biosecurity are often conducted in secret. Even in the United States, there is no coordinated approach to laboratory biosafety or reporting laboratory accidents. As a result, public awareness of biosafety incidents often relies on local engagement between towns and specific labs, or comes from journalists filing Freedom of Information requests. The U.S. Government Accountability Office has consistently criticized U.S. biological security and safety for decades, but even recent developments in regulating the funding of potentially high-consequence gain of function research have been criticized as lacking transparency around the makeup of the review board, decision-making procedure, and notification of funded experiments. If this is the case for the United States, it is easy to imagine that other countries with less experience with biosafety and security might see it as politically advantageous to remain mum about incidents or problems. Clearly, more work is needed around the world to make sure that all countries have biorisk management policies and appropriate oversight measures in place, and that theyre open about the problems they encounter and their efforts to solve them.

Global norms and incentives are where the rubber hits the road for pandemic preparedness. Its reasonable in fact, vital to seek new ways to prevent laboratory accidents in the future. The worlds chief solution to this pandemic was the development of vaccines, a process driven by life sciences research, much of which took place in high-containment labs. Consequently, many political leaders may well choose to invest in more high-level biological research in the near future. If the solution to a lab release is more laboratory science, it makes sense to ensure that that science is carried out in a safe and secure manner. There is room for all countries to do better, and the United States should consider revitalizing its approach to promoting biosafety and biosecurity in the wake of the pandemic regardless of its origins.

As a final point, if the lab release hypothesis is true, we really shouldnt be surprised. An analysis in 2016 of gain of function research by Gryphon Scientific operated on the assumption that, eventually, a laboratory release of a potential pandemic pathogen would occur, a small number of those would lead to a local cluster, and a small number of those would seed a global pandemic. In other words, if COVID-19 did result from a lab release in China, it might simply have been bad luck, on top of whatever biosafety lapses China may have had which is all the more reason why, in addition to strengthening laboratory safety and security, the international community should do everything it can to develop appropriate infrastructure to handle a future pandemic.

Looking Ahead

There is one important scenario in which it would be absolutely vital to know the origins of COVID-19 in order to decide what to do next. If, as some scientists and politicians have suggested, the pandemic stemmed from a deliberate attempt to develop a biological warfare agent, this would have serious implications for the Biological Weapons Convention and the broader norm against the use of disease as a weapon. If a state party had violated its commitment to the treaty by developing biological weapons, the international community would need to determine how to hold that government accountable for its non-compliance a process with which states parties to the treaty have struggled in the past. Even treaties that have extensive verification provisions have grappled with what to do when a state party has demonstrably violated a treatys prohibitions. While some might criticize the Biological Weapons Convention for lacking a mechanism to verify compliance, such mechanisms dont solve the knotty political problem of what to do when flagrant violations take place. Moreover, the deliberate use of biological weapons could inspire copycat behavior by others, leading to the weakening of the norm against the use of disease as a weapon. Fortunately, to our knowledge no serious analysis of COVID-19s origins even from those who support a laboratory release hypothesis has concluded that anyone deliberately introduced the SARS-CoV-2 virus to the global population.

While its important to discover the origins of the pandemic, theres a danger in taking these efforts too far. Some have argued that conclusively demonstrating the pandemics origins in a lab release might help nations seeking to encourage China to pay financial reparations for the global economic cost of the virus to make their case. This could be a problematic approach. Not only is there no legal precedent under international law to hold a country liable for a pandemic, but in the long run this might be an unwise road for the United States, given its own history of laboratory accidents and safety lapses. Insisting that China bears responsibility for the pandemic and should be expected to pay compensation to other countries or the families of coronavirus victims could backfire in the future if the United States finds itself attempting to mitigate the consequences from a laboratory accident. Furthermore, legal efforts to blame China could fuel additional xenophobia against Asian-Americans, or even undermine U.S. foreign policy interests.

Meanwhile, the focus on where the virus came from should not divert attention from whats even more important preparing for the next pandemic. Political finger-pointing might make it far more difficult for researchers to collaborate internationally on pandemic preparedness efforts. Experts are already noting the possible implications for the National Institutes of Health and other research institutions of the growing tension between the United States and China, exacerbated by the allegations and skepticism around the viruss origins. This pandemic is far from over, despite the rollout of vaccines in the United States, and new potential pandemic diseases are already testing global health efforts elsewhere in the world. American experts therefore need to keep a laser-like focus on the real enemy: the causative agents of disease.

There will be far more blame to share if the international community becomes so fixated on the circumstances surrounding this unique case that its unable to see the big picture and predict or prepare for the next pandemic. Theres work that can be done in that respect while maintaining agnosticism about the origins of COVID-19. Regardless of the source, we need to be better prepared to respond to the next virus.

Amanda Moodie is a policy fellow at the National Defense Universitys Center for the Study of Weapons of Mass Destruction (WMD Center) in Washington, D.C. Her policy support at the center focuses on the international legal regimes that regulate the proliferation of chemical and biological weapons. She regularly serves as a member of the U.S. delegation to meetings of the states parties of the Biological Weapons Convention.

Nicholas G. Evans is an assistant professor in the Department of Philosophy at the University of Massachusetts Lowell, where he teaches biomedical ethics and security studies. He has been published in the British Medical Journal, Nonproliferation Review, and ELife. His book, The Ethics of Neuroscience and National Security, was released with Routledge in May 2021.

The views expressed in this paper are those of the authors and are not an official policy or position of the National Defense University, the Department of Defense, or the U.S. government.

Image: Xinhua (Photo by Fei Maohua)

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The Origin of COVID-19 and Preventing the Next Pandemic - War on the Rocks

COVID-19 Vaccination Hesitancy Finds Echo in Cancer Care – OncLive

Unfortunately, not all people recognize this success or the need for vaccines that prevent infections with these dangerous pathogens. The history of vaccination hesitancy is long. In much earlier times, there was legitimate concern for both the safety and efficacy of proposed vaccine products due to the lack of a rigorous clinical trials process and formal regulatory review by experts in vaccine science, epidemiology, and statistical analysis. More recently, however, with our far greater understanding of the biology of infectious diseases, the establishment of robust and well-validated clinical trial strategies for evaluating vaccine products and scrupulous review by both governmental health agencies and external experts, the utility of a given vaccine is clear before it is approved. Mandatory reporting of adverse effects following use in the real world ensures that rare or longer-term concerns are appropriately evaluated.

Consider, for example, findings from a recent review of 57 vaccines that the FDA approved from January 1, 1996, to December 31, 2015. More than 90% of the vaccines were supported by data from randomized controlled trials, each involving a median of more than 4100 study participants.4 The authors noted that the postsurveillance mechanism worked well, with a total of 58 safety-related modifications added to the FDA-approved vaccine labels involving approximately half of the vaccines (n = 25). Most of the changes related to additional warnings that stemmed from extended experience with the vaccine. A total of 8 contraindications were added to the labels, and only 1 vaccine product was withdrawn from the market due to safety-related issues.

Restrictions on the patient populations who should be eligible to receive the vaccine was the most common change mandated by the FDA, with additional notification regarding potential allergic reactions being the second most common issue arising from follow-up review. The investigators concluded: Over a 20-year period, vaccines were found to be remarkably safe. A large proportion of safety issues were identified through existing postmarketing surveillance programs and were of limited clinical significance. These findings confirm the robustness of the vaccine approval system and postmarketing surveillance.4

Following the introduction of several COVID-19 vaccines, there were reports of a rare blood-clotting disorder associated with at least 2 of the products in noninvestigative real-world use. The events were quickly evaluated, with public health agencies making recommendations for the future delivery of these vaccines. Although the COVID-19 vaccine rollout is unprecedented in speed and scope, the process of postapproval surveillance has been shown to be robust and should serve as a source of reassurance to the public regarding the effectiveness of the initial and follow-up review process.

Unfortunately, this is an oversimplified view of the entire spectrum of the vaccination process. In a most provocative commentary, Naomi Oreskes, PhD, a professor of the history of science at Harvard University, noted that we should perhaps reassess the nature of the difficulty associated with developing and implementing an effective vaccination strategy.5 The author highlights the fact we have traditionally considered problems to be hard that are associated with major technological challenges or an understanding of highly complex theories (eg, quantum physics). The development of several highly effective COVID-19 vaccines and their release for noninvestigative administration less than 1 year follow-ing the identification of the molecular structure of the causative virus is nothing short of remarkable, yet we have struggled until recently to implement a nationwide vaccine distribution strategy. What good is a vaccine that remains in a vial rather than being injected into the arm of an individual susceptible to a COVID-19 infection?

Oreskes concludes: We call the physical sciences hard because they deal with issues that are mostly independent of the vagaries of human nature; they offer laws that (at least in the right circumstances) yield exact answers. But physics and chemistry will never tell us how to design an effective vaccination programin part because they do not help us comprehend human behavior. The social sciences rarely yield exact answers. But that does not make them easy.5

Although the COVID-19 vaccines must be regarded as truly remark-able scientific success stories,6 we are faced with the reality of human behavior, and we are learning that overcoming obstacles to existing and firmly entrenched beliefs, reinforced by social media sources and conspiracy theories, will be hard.7,8

We should recognize that this conclusion also pertains to the admin-istration of vaccines that have been documented to be both safe and highly effective in the prevention of cancer. We now have conclu-sive evidence that vaccination against the human papillomavirus (HPV) can substantially reduce the risk of developing invasive cervi-cal cancer.9 However, recent self-reported data reveal that, among 12,644 women and men aged 18 to 21 years in the United States, only 55% of women and 34% of men had received at least 1 dose of the HPV vaccine.10 Clearly, we have a long way to go to solve this hard prob-lem of increasing the delivery of this critically important cancer prevention strategy.

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COVID-19 Vaccination Hesitancy Finds Echo in Cancer Care - OncLive

Odds and Ends: Knowing the Difference Between Sports Fandom and Toxicity – SportsRaid

The NBA Playoffs are here so you know this is the time when weird, out there news takes over the cycle in conjunction with the actual games. You dont know why this happens. It just does for whatever reason. The latest discussion happening in the discourse is in response to fandom and how they act during games.

So recently Atlanta Hawks All Star point guard Trae Young has joined the ranks of Reggie Miller, Michael Jordan, Scottie Pippen, Isiah Thomas, and Paul Pierce as the latest edition of Knicks Killers, supervillains who were created for the sole purpose of ruining the New York Knickerbockers chances of postseason success. To be honest, thats quite an honor! Young has even acknowledged it! His Game 1 performance was a spectacle that showcased a young star player embracing his role as the bad guy against a rival team and it was fun (if youre a Hawks fan)!

What was not fun was the ensuing vitrol and mistreatment Young and his family has received after the game. Shouting f*** Trae Young, making fun of his height and hair is all over-the-top jeering that would not be out of place in an NBA Playoff atmosphere but the fan who was trying to spit at him crossed the line, which is a disgusting display of human behavior.

I definitely didnt see it, but theres no place for that, man, Knicks All Star Julius Randle said to reporters after the incident. I dont care if its our home crowd or not, theres no place for that. Weve got to protect the players. Thats disrespectful. Yeah, its our fans and I love our fans, but you see a guy on the street, you wouldnt spit on him. You wouldnt disrespect somebody like that. I dont care what arena its in, whose fan base it is, theres absolutely no place for disrespecting anybody in any capacity and especially spitting on him. Thats just ridiculous.

It has been happening through out much of the NBA postseason. Fans have been welcomed back to the arenas after being away for more than a year due to the COVID-19 Pandemic. However in true entitled, idiotic fashion fans have been abusing players by either hurling personal attacks on players families and friends, throwing bottles, or attempting to disrupt a game by running on the court, endangering the players on the floor.

Sheesh NBA fans cant have nothing.

Look, I get it. People have been locked up in their homes for over a year. It has been a struggle trying to re-experience social norms and nobody knows when this pandemic is going to end. Sure, vaccines are readily available and the numbers of those infected by the virus have decreased over time but that does not give people the right to mistreat others, especially those who are out there providing entertainment in the world of sports.

The idiot nature of those attempting to commit actual harm to NBA athletes and those mocking athletes with nonsensical chants should not be perceived as the same. If you chant Julius Randle is overrated! then that is not exactly a harmful insult considering the season Randle had and trust he has heard worst. However, if you throw insults at Randles wife and son then you are crossing the line. You made the matter personal and have put someones well-being in danger.

Fans have rights to jeer at athletes. It is all part of the fun within the playoffs. However, people should be mindful as to how they carry themselves. That type of behavior is unacceptable and the NBA should continue to hold those fans accountable for their actions. It is impossible to police human behavior considering that nobody not even the arena personnel can keep those type of people in check. I mean it is not like you can ban 15,000 people out of a game if they all chant Kyrie sucks! In any case, people need to learn to relax and enjoy the game.

To quote the great Kevin Wayne Durant, Have some respect for the human beings and have some respect for yourself. Your mother wouldnt be proud of you throwing water bottles at basketball players or spitting on players or tossing popcorn. So grow the f up and enjoy the game, its bigger than you.

*additional content from Sporting News, House of Highlights, ESPN, NBA on TNT, Bleacher Report, NY Post

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Odds and Ends: Knowing the Difference Between Sports Fandom and Toxicity - SportsRaid

Why does the coronavirus change? – Khmer Times

Variants of viruses occur when there is a change or mutation to the viruss genes. Ray says it is the nature of RNA viruses such as the coronavirus to evolve and change gradually. Geographic separation tends to result in genetically distinct variants, he says.

Mutations in viruses including the coronavirus causing the COVID-19 pandemic are neither new nor unexpected. Bollinger explains: All RNA viruses mutate over time, some more than others. For example, flu viruses change often, which is why doctors recommend that you get a new flu vaccine every year.

Is there a new coronavirus mutation?We are seeing multiple variants of the SARS-CoV-2 coronavirus that are different from the version first detected in China, Ray says.

He notes that one mutated version of the coronavirus was detected in southeastern England in September 2020. That variant, now known as B.1.1.7, quickly became the most common version of the coronavirus in the United Kingdom, accounting for about 60% of new COVID-19 cases in December. It is now the predominant form of the coronavirus in some countries.

Different variants have emerged in Brazil, California and other areas. A variant called B.1.351, which first appeared in South Africa, may have the ability to re-infect people who have recovered from earlier versions of the coronavirus. It might also be somewhat resistant to some of the coronavirus vaccines in development. Still, other vaccines currently being tested appear to offer protection from severe disease in people infected with B.1.351.

B.1.351: A Coronavirus Variant of Concern?One of the main concerns about the coronavirus variants is if the mutations could affect treatment and prevention.

The variant known as B.1.351, which was identified in South Africa, is getting a closer look from researchers, whose early data show that the COVID-19 vaccine from Oxford-AstraZeneca provided minimal protection from that version of the coronavirus. Those who became sick from the B.1.351 coronavirus variant after receiving the Oxford-AstraZeneca vaccine experienced mild or moderate illness.

The B.1.351 variant has not been shown to cause more severe illness than earlier versions. But there is a chance that it could give people who survived the original coronavirus another round of mild or moderate COVID-19.

Researchers studying placebo (non-vaccine) recipients in the South African COVID-19 vaccine trial by Novavax compared subgroups of participants who did or did not have antibodies indicating prior COVID-19. Those who did have the antibodies most likely were infected with older variants of SARS-CoV-2. They found that having recovered from COVID-19 did not protect against being sickened again at a time when the B.1.351 variant was spreading there.

Will the COVID-19 vaccine work on the new variants?Ray says, There is new evidence from laboratory studies that some immune responses driven by current vaccines could be less effective against some of the new strains. The immune response involves many components, and a reduction in one does not mean that the vaccines will not offer protection.

People who have received the vaccines should watch for changes in guidance from the CDC [Centers for Disease Control and Prevention], and continue with coronavirus safety precautions to reduce the risk of infection, such as mask wearing, physical distancing and hand hygiene.

We deal with mutations every year for flu virus, and will keep an eye on this coronavirus and track it, says Bollinger. If there would ever be a major mutation, the vaccine development process can accommodate changes, if necessary, he explains.

How are the new coronavirus variants different?There are 17 genetic changes in the B.1.1.7 variant from England, Bollinger says. Theres some preliminary evidence that this variant is more contagious. Scientists noticed a surge of cases in areas where the new strain appeared.

He notes that some of the mutations in the B.1.1.7 version seem to affect the coronaviruss spike protein, which covers the outer coating of SARS-CoV-2 and give the virus its characteristic spiny appearance. These proteins help the virus attach to human cells in the nose, lungs and other areas of the body.

Researchers have preliminary evidence that some of the new variants, including B.1.1.7, seem to bind more tightly to our cells Bollinger says. This appears to make some of these new strains stickier due to changes in the spike protein. Studies are underway to understand more about whether any of the variants are more easily transmitted.

Are coronavirus variants more dangerous?Bollinger says that some of these mutations may enable the coronavirus to spread faster from person to person, and more infections can result in more people getting very sick or dying. In addition, there is preliminary evidence from Britain that some variants could be associated with more severe diseases. Therefore, it is very important for us to expand the number of genetic sequencing studies to keep track of these variants, he says.

Bollinger explains that it may be more advantageous for a respiratory virus to evolve so that it spreads more easily. On the other hand, mutations that make a virus more deadly may not give the virus an opportunity to spread efficiently. If we get too sick or die quickly from a particular virus, the virus has less opportunity to infect others. However, more infections from a faster-spreading variant will lead to more deaths, he notes.

Could a new COVID-19 variant affect children more frequently than earlier strains?Ray says that although experts in areas where the new strain is appearing have found an increased number of cases in children, he notes that the data show that kids are being infected by old variants, as well as the new ones. There is no convincing evidence that any of the variants have special propensity to infect or cause disease in children. We need to be vigilant in monitoring such shifts, but we can only speculate at this point, he says.

Will there be more new coronavirus variants?Yes. As long as the coronavirus spreads through the population, mutations will continue to happen.

New variants of the SARS-CoV-2 virus are detected every week, Ray says. Most come and go some persist but dont become more common; some increase in the population for a while, and then fizzle out. When a change in the infection pattern first pops up, it can be very hard to tell whats driving the trend changes to the virus, or changes in human behavior. It is worrisome that similar changes to the spike protein are arising independently on multiple continents.

Are there additional COVID-19 precautions for the new coronavirus mutations?Bollinger says that as of now, none of the new coronavirus variants call for any new prevention strategies. We need to continue doing what were doing, he says.

Ray concurs: There is no demonstration yet that these variants are biologically different in ways that would require any change in current recommendations meant to limit spread of COVID-19, he says. Nonetheless, we must continue to be vigilant for such phenomena.

Ray stresses that human behavior is important. The more people who are infected, the more chances there are for a mutation to occur. Limiting the spread of the virus through maintaining COVID-19 safeguards (mask wearing, physical distancing and practicing hand hygiene) gives the virus fewer chances to change. It also reduces the spread of more infectious variants, if they do occur.

We need to re-emphasize basic public health measures, including masking, physical distancing, good ventilation indoors and limiting gatherings of people in close proximity with poor ventilation. We give the virus an advantage to evolve when we congregate in more confined spaces, he says.

Regarding coronavirus variants, how concerned should we be?Most of the genetic changes we see in this virus are like the scars people accumulate over a lifetime incidental marks of the road, most of which have no great significance or functional role, Ray says. When the evidence is strong enough that a viral genetic change is causing a change in the behavior of the virus, we gain new insight regarding how this virus works.

As far as these variants are concerned, we dont need to overreact, Bollinger says. But, as with any virus, changes are something to be watched, to ensure that testing, treatment and vaccines are still effective. The scientists will continue to examine new versions of this coronaviruss genetic sequencing as it evolves.

In the meantime, we need to continue all of our efforts to prevent viral transmission and to vaccinate as many people as possible, and as soon as we can. Hopkins Medicine

Originally posted here:
Why does the coronavirus change? - Khmer Times

NSBORO Roundup: Masks not required outdoors; Studying the Holocaust; Start Time Reminder; and No to School Choice – mysouthborough

Im rounding up some of the school related news I missed sharing recently. Some stories are from the media and others from school announcements.

Outdoor Mask Requirement lifted for elementary schools NSBORO District:

When the district announced on May 19th that masks would still be required during recess at NSBORO elementary schools, some parents objected. At the time, the Medical Advisory Team noted that they would continue to look at the data weekly and make adjustments. It appears that they did just that.

The Districts website includes the following messageto parents of PreK-5 students of a new policy that went into effect yesterday:

Beginning on June 1, 2021, and in alignment with Governor Bakers shifting the states mask mandate to a mask advisory, and the Department of Elementary and Secondary Educations updated mask guidelines, the Public Schools of Northborough and Southborough will no longer require that masks be worn by students when outdoors during recess, physical education or outdoor classroom environments, even when social distance can not be maintained. Masks are required on the bus at all times and inside the school buildings, except when eating.

In alignment with the Center for Disease Control (CDC) guidelines*, The Public Schools of Northborough and Southborough strongly encourages all non-vaccinated persons to wear masks outdoors when they are with individuals from outside their household and unable to maintain social distance. The Medical Advisory Team supports mask wearing for non-vaccinated students. (read more)

Northborough HS Class Takes Deep Dive Into What Led To The Holocaust CBS Boston:

Local broadcast news covered a Social Studies elective at the high school. (Although, the headline ignores the Regional part of Algonquins name.)

Most kids learn about the Holocaust in school, but Algonquin Regional High School in Northborough is taking it one step further with lessons on human behavior.

I think its really helped me to understand why my family was killed, said Jordan Chastanet, a senior at Algonquin.

The course is called Holocaust & Human Behavior. The elective, which is offered to juniors and seniors, is more than just a class. Its personal.

My grandmother was actually a Holocaust survivor, and two of her sisters and her escaped from the Warsaw ghetto. And Ive heard so much about my history, said Chastanet. (read and view more)

(You can also find the full course description in Algonquins Program of Studies.)

Start Time Update Planning forthe 2021-2022 School Year NSBORO District:

Recent updates from the Superintendent remind parents and students to prepare for changing start times for schools this fall.

The initiative to allow Algonquin students sleep later resulted in a radically revised 2-tiered bus schedule. Most students schools times will start and end later, except for Trottier Middle School. (The 6th-8th graders will actually start and end 13 minutes earlier.) Below is an excerpt from the update in the May newsletter with the table of Southborough start times:

Northborough & Southborough School Districts opt-out of school choice Community Advocate:

It looks like there were no surprises in the school committee votes on School Choice. As usual, all three NSBORO districts chose not to accept students from outside the district:

The Northborough-Southborough Regional School Committee unanimously voted to opt-out of the inter-district school choice program at their meeting May 19.

This decision aligns with the vote of both the Northborough K-8 and Southborough K-8 School Committee.

Although there are some advantages to school choice, such as a means to generate revenue and allow for flexibility in enrollment declines, Superintendent Greg Martineau cited disadvantages.

He explained the $5,000 in tuition the district would receive for each student would be far less than the districts per-pupil expenditure of $18,621.13 based on fiscal year (FY)2020.

The fall reopening of schools was also a concern for Martineau.

Theres no need to add another variablein terms of what the fall may look like, he said. (read more)

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NSBORO Roundup: Masks not required outdoors; Studying the Holocaust; Start Time Reminder; and No to School Choice - mysouthborough

DNA Markers Uncovered in Grape Genetics Research Reveal What Makes the Perfect Flower – SciTechDaily

Flower sex is an important factor when breeding for quality cultivars.

Wines and table grapes exist thanks to a genetic exchange so rare that its only happened twice in nature in the last 6 million years. And since the domestication of the grapevine 8,000 years ago, breeding has continued to be a gamble.

When todays growers cultivate new varieties trying to produce better-tasting and more disease-resistant grapes it takes two to four years for breeders to learn whether they have the genetic ingredients for the perfect flower.

Females set fruit, but produce sterile pollen. Males have stamens for pollen, but lack fruit. The perfect flower, however, carries both sex genes and can self-pollinate. These hermaphroditic varieties generally yield bigger and better-tasting berry clusters, and theyre the ones researchers use for additional cross-breeding.

Now, Cornell scientists have worked with the University of California, Davis, to identify the DNA markers that determine grape flower sex. In the process, they also pinpointed the genetic origins of the perfect flower. Their paper, Multiple Independent Recombinations Led to Hermaphroditism in Grapevine, published on April 13, 2021, in the Proceedings of the National Academy of Science.

This is the first genomic evidence that grapevine flower sex has multiple independent origins, said Jason Londo, corresponding author on the paper and a research geneticist in the USDA-Agricultural Research Service (USDA-ARS) Grape Genetics Unit, located at Cornell AgriTech. Londo is also an adjunct associate professor of horticulture in the School of Integrative Plant Science (SIPS), part of the College of Agriculture and Life Sciences.

This study is important to breeding and production because we designed genetic markers to tell you what exact flower sex signature every vine has, Londo said, so breeders can choose to keep only the combinations they want for the future.

Today, most cultivated grapevines are hermaphroditic, whereas all wild members of the Vitis genus have only male or female flowers. As breeders try to incorporate disease-resistance genes from wild species into new breeding lines, the ability to screen seedlings for flower sex has become increasingly important. And since grape sex cant be determined from seeds alone, breeders spend a lot of time and resources raising vines, only to discard them several years down the line upon learning theyre single-sex varieties.

In the study, the team examined the DNA sequences of hundreds of wild and domesticated grapevine genomes to identify the unique sex-determining regions for male, female and hermaphroditic species. They traced the existing hermaphroditic DNA back to two separate recombination events, occurring somewhere between 6 million and 8,000 years ago.

Londo theorizes that ancient viticulturists stumbled upon these high-yielding vines and collected seeds or cuttings for their own needs freezing the hermaphroditic flower trait in domesticated grapevines that are used today.

Many wine grapes can be traced back to either the first or second event gene pool. Cultivars such as cabernet franc, cabernet sauvignon, merlot, and Thompson seedless are all from the first gene pool. The pinot family, sauvignon blanc, and gamay noir originate from the second gene pool.

What makes chardonnay and riesling unique is that they carry genes from both events. Londo said this indicates that ancient viticulturalists crossed grapes between the two gene pools, which created some of todays most important cultivars.

Documenting the genetic markers for identifying male, female and perfect flower types will ultimately help speed cultivar development and reduce the costs of breeding programs.

The more grape DNA markers are identified, the more breeders can advance the wine and grape industry, said Bruce Reisch, co-author and professor in both the Horticulture and the Plant Breeding and Genetics sections of SIPS. Modern genetic sequencing technologies and multi-institutional research collaborations are key to making better grapes available to growers.

Reference: Multiple independent recombinations led to hermaphroditism in grapevine by Cheng Zou, Mlanie Massonnet, Andrea Minio, Sagar Patel, Victor Llaca, Avinash Karn, Fred Gouker, Lance Cadle-Davidson, Bruce Reisch, Anne Fennell, Dario Cantu, Qi Sun and Jason P. Londo, 9 April 2021, Proceedings of the National Academy of Sciences.DOI: 10.1073/pnas.2023548118

Funding for this study was provided by a Specialty Crop Research Initiative Competitive Grant from the USDA National Institute of Food and Agriculture.

Co-authors on the paper also include Cheng Zou and Qi Sun at the Cornell Institute of Biotechnology; Melnie Massonnet, Andrea Minio and Dario Cantu at UC Davis; Lance Cadle-Davidson at the USDA-ARS Grape Genetics Unit; Victor Llaca at Corteva Agriscience; Avinash Karn and Fred Gouker in the Horticulture Section of SIPS; and Sagar Patel and Anne Fennell of South Dakota State University.

Erin Rodger is the senior manager of marketing and communications for Cornell AgriTech.

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DNA Markers Uncovered in Grape Genetics Research Reveal What Makes the Perfect Flower - SciTechDaily

Research on Bizarre Rodent Genetics Solves a Mystery And Then Things Got Even Stranger – SciTechDaily

A Taiwan vole, closely related to the creeping vole described in the study. Credit: Lai Wagtail / Flickr (CC BY-NC-ND 2.0)

Open up Scott Roys Twitter bio and youll see a simple but revealing sentence: The more I learn the more Im confused. Now the rest of the scientific world can share in his confusion. The San Francisco State University associate professor of Biologys most recent research, published earlier this month in one of the scientific worlds most prestigious journals, catalogues a strange and confounding system of genes in a tiny rodent that scientists have ignored for decades.

This is basically the weirdest sex chromosome system known to science, Roy said. Nobody ordered this. But hes serving it anyway.

The owner of those chromosomes is the creeping vole, a burrowing rodent native to the Pacific Northwest. Scientists have known since the 60s that the species had some odd genes: Their number of X and Y chromosomes (bundles of DNA that play a large role in determining sex) is off from whats expected in male and female mammals.

That finding caught Roys eye when presented by a guest speaker at a San Francisco State seminar, and he realized that modern technology might be able to shed new light on the mysteries hiding in the voles DNA. After working with collaborators to disentangle the voles genetic history resulting in one of the most completely sequenced mammal genomes that exists, according to Roy the story only got stranger.

The team found that the X and Y chromosomes had fused somewhere in the rodents past, and that the X chromosome in males started looking and acting like a Y chromosome. The numbers of X chromosomes in male and female voles changed too, along with smaller pieces of DNA getting swapped between them. The researchers published their results in Science on May 7, 2021.

Drastic genetic changes like these are exceptionally rare: The way genes determine sex in mammals has stayed mostly the same for about 180 million years, Roy explains. Mammals, with few exceptions, are kind of boring, he said. Previously we would have thought something like this is impossible.

So how did the genes of this unassuming rodent end up so jumbled? Its not an easy question to answer, especially since evolution is bound to produce some strangeness simply by chance. Roy, however, is determined to figure out the why. He suspects that what the team found in the voles genome is something like the aftermath of an evolutionary battle for dominance between the X and Y chromosome.

The research couldnt have happened, Roy says, without collaborations with Oregon fish and wildlife biologists who had a creeping vole sample sitting in a lab freezer. He also teamed up with a group from Oklahoma State University when the two groups started chatting about creeping vole DNA sequences that were posted on the internet and both realized they were working on the same question.

Another key was working at a teaching-focused institution. Roy says he has the time to develop ideas with colleagues and students at SF State, and he can do research where he doesnt quite know what hell find. This is a great example of non-hypothesis-based biology, Roy explained. The hypothesis was, This system is interesting. I bet if you looked into it some more, thered be other interesting things.

It wont be the last time Roys lab goes out on a limb. He and his collaborators plan to look into the genomes of other species related to the voles to chart the evolutionary path that led to this strange system. Hell also continue DNA sequencing curiosities across the tree of life.

These bizarre systems give us a handhold to start to understand why the more common systems are the way they are and why our biology works as it does, he explained. By delving into the weirdest that nature has to offer, maybe we can come to understand ourselves better, too.

Reference: Sex chromosome transformation and the origin of a male-specific X chromosome in the creeping vole by Matthew B. Couger, Scott W. Roy, Noelle Anderson, Landen Gozashti, Stacy Pirro, Lindsay S. Millward, Michelle Kim, Duncan Kilburn, Kelvin J. Liu, Todd M. Wilson, Clinton W. Epps, Laurie Dizney, Luis A. Ruedas and Polly Campbell, 7 May 2021, Science.DOI: 10.1126/science.abg7019

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Research on Bizarre Rodent Genetics Solves a Mystery And Then Things Got Even Stranger - SciTechDaily